The objective of this study is to completely define the chemical requirements for induction in rats of both hyperacute and ordinary experimental autoimmune encephalomyelitis (EAE). The minimum length(s) of the(se) determinant(s) within guinea pig basic protein will be ascertained by solid phase peptide synthesis. Single amino acid substitutions will be made in this site(s) synthetically in order to evaluate the contribution of each amino acid to the disease process. This project will determine whether hyperacute and ordinary EAE differ because of separate encephalitogenic determinants, acting either independently or in synergy, or whether a separate, nonencephalitogenic, determinant is acting as a carrier molecule promoting a different, perhaps IgE mediated, immune response to a single encephalitogenic determinant common to all species.